The cellular mechanisms responsible for the tumor promoting effects of renal and hepatic tumor promoters are under investigation in rodents. We previously established that the renal tumor promoter and former human drug, barbital sodium, stimulates the growth of preneoplastic renal tubular cell foci initiated by genotoxic carcinogens (see also project ZOICPO5299). Enhancement of these foci to progress to adenoma and carcinoma is a major effect of barbital sodium. The relationship between the target organ toxicity of the barbital, renal tubular hyperplasias and neoplasms, is under study. Barbital, itself, was found to be a relatively "weak" carcinogen for rat kidney. In the rat liver, using naturally-occurring or carcinogen-initiated glutathione S-transferase, placental form (GSTP) single immunoreactive hepatocytes as putative initiated cells, the nongenotoxic hepatocarcinogen, di(2-ethylhexyl)phthalate (DEHP), a peroxisomal proliferator, could not promote these cells to develop into hepatic tumors.